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Week 4 - Han and Yiu

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Both papers this week discuss the existence of and the ability to manipulate memory localization in the brain. The 2009 Han et al article seeks to find out if killing the neurons that are activated during a given fear memory erase the memory. It was discovered that when a specific set of neurons in the Lateral Amygdala (LA) that have higher CREB concentrations were killed, the corresponding auditory fear memory was suppressed. Yiu et al’s 2014 article builds off of Han’s research to understand why this happens and to see if this stays true in neurons of different areas of the brain. This team confirms Han’s findings and reveals that the strength of the connection between a neuron and a memory is not necessarily dependent on CREB levels but is dependent on the neuron’s prior excitability. I agree that Han’s study was too minimal and I was left feeling unsatisfied with many questions as to how and why CREB levels affect memory in this way. Yiu not only tackled this question but also tested more areas in the amygdala to confirm this only occurs in the LA and controlled for anxiety levels through the OFT and EPT. 

 It interests me how memory is discussed here as such a physical set of connections, although I suppose this is the nature of neuroscience. In most of the research I have read, memory is more of an abstract concept that is measured in terms of behavioral output. This is especially true when it comes to memory localization and different types of memory. This paper seems to take this a step further and pinpoint exactly which neurons carry a specific memory. There would be significant and obvious clinical benefits to this type of research – the identification and removal of fear memory – especially in people with PTSD and perhaps depression and anxiety. However, although the removal of harmful fear memory sounds great, killing any part of the human brain would be dangerous and difficult to do successfully. It would take more research into the role of these neurons and the consequence of removing them before this method could be used therapeutically. Perhaps there is a way to, instead of killing them, alter their excitability or increase inhibition for a certain amount of time. 

 These research papers also make me think about the complexity and convoluted nature of memory and how several neurons can be responsible for the trace of many memories at the same time. This is something to keep in mind when killing neurons in live patients – it may affect more than just the one memory. I would be interested in further research on if this phenomenon also occurs with other types of memories, such as happy and sad ones, in other areas of the brain. Perhaps altering the activation of these neurons affects mood and depressive behavior. Even if this is true in rats, I think it would be a long time until this research is clinically applicable in humans.

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